The consequences of a week of insomnia. II: Patients with insomnia.

Insomnia patients present with a consistent set of complaints that they generally report as secondary to their poor sleep, including increased tension/confusion, decreased vigor, personality disturbance, subjective overestimation of poor sleep, increased body temperature, increased 24-hour whole-body metabolic rate, and longer MSLT latencies. If there is a relationship between the poor sleep and the secondary symptoms, then particularly poor sleep should exacerbate those symptoms. Ten patients with insomnia were identified on the basis of a 2-night screening protocol, then slept in the laboratory for 10 additional nights. On 7 of the nights, the insomnia patients had their wake-after-sleep-onset increased so that their total sleep time was 80% of that on their second screening night, resulting in an average of 254 minutes (of 480 minutes in bed) of sleep. The spectrum of changes seen in these patients with insomnia who had very poor sleep for a week was characteristic of mild partial sleep deprivation, and not consistent with exacerbation of symptoms found in patients with primary insomnia. Specifically, (1) these patients had a reduction as opposed to an increase in the MSLT values, but the MSLT values at the end of the week remained within normal limits; (2) these patients had decreased (as opposed to increased) whole metabolic rate following nights of particularly poor sleep; (3) these patients tended to underestimate (rather than overestimate) their subjective sleep latency while being given particularly poor sleep; and (4) these patients displayed no significant change in body temperature, subjective anxiety, or MMPI scores following particularly poor sleep. It was concluded that the secondary symptoms reported by patients with primary insomnia are probably not related to their poor sleep per se. Data from previous studies that varied physiological arousal were used to support the contention that the secondary symptoms of patients with insomnia, and perhaps the poor sleep itself, occur secondary to central nervous system hyperarousal.